Derm Flashcards
atopic dermatitis (AD, eczema) causes
genetic + environmental causes
results from abnormal epidermal barrier fx
Environment
- drying agents: prolonged baths, soap, shampoo, chloride in pools
- abrasive clothes: wool, nylon, acrylic (need 100% cotton)
- abrasive surfaces: carpet, sandpits, lamb wool covers, parent clothes
- heat (only if active eczema)
- chemicals: fragrances, preservatives
- staph aureus colonidation → can exacerbvate inflammatory process by super antigen effect, resulting in reduced response to steroids
allergy is involved in MINORITY of patients
AD clinical features
itchy rash
most kids will present by 12 mo, usually appears at 3-4 months old
distribution: starts mainly in head +/- trunk +/- limbs
can get flexure (popliteal, axilla, elbow + ankle flexors) involvement <12 mo
scalp common
if becomes chronic inflammation → lichenification of skin
most kids get gradual improvment with time
other types
- pompholyx of hands/soles = blistering manifestaiton can get desquamation
- often isolated to hands/soles
- high risk of occupational hand ezcema as adult
- need counselling!
Foods commonly causing IgE-mediated reactions.
What is the natural Hx
COMMON FOOD CAUSES:
>90% of clinical reactions caused by:
Cow’s mik
Egg
Peanut (NB: is a legume, NOT a nut)
→ peanut is the food most likely to cause severe or fatal anaphylaxis (peanut allergens are heat stable)
→ increased risk of allergy to true nuts egt: cashew, almond, hazelnut + walnut
→ almost all children w fatal anaphylaxis had significant PMHx asthma
NB: reactions often specific for individual w fish or shellfish
ANY protein containing food (esp if rich) can be allergenic
NATURAL Hx
most immediate food hypersensitivities ( IgE + non-IgE mediated) diminish w time
- esp cow milk + egg
peanut, nuts, fish + shellfish allergies → more likely to PERSIST into adulthood
in generally cooking makes foods less allergenic
Allergic reaction - what mediators released early and late in reactions?
Early/immediate
degranulation of mast cells
- histamines++++
+ leukotrienes + cytokines + proteases
later secretion of
- cytokines and chemokines
Dx of food allergy
Hx is VERY important
Demonstrate IgE mediated Dz
- Skin prick test (often better) vs serum specific IgE testing (RAST)
- RAST wont be +ve if not IgE mediated (ie: needs to be an immediate reaction, not >2hrs = non-IgE mediated)
- NB: +ve test does NOT necessarily mean food is responsible for reaction.
If strong Hx + strong IgE = highly predictive
Best way is to challenge but may be dangerous
NB: negative result despite convincing Hx → seen in younger infants OR primarily GIT reactions (esp cow milk. soy, rice, other grains)
Mx allergy
Avoidance
dietetic advice
explain excellent prognosis for spontaneous resolution in most foods
yearly r/w +/- repeat testing in uncomplicated cases
NB:where risk of severe reactions (esp resp compromise or Hx of asthma esp w nut allergy)
→ prescribe Epipen! + educate on use
Allergic reaction + anaphylaxis action plans ESSENTIAL
Which infant at high risk of developing allergy? What prevention strategies are there for them?
both parents atopic 40 - 60%
both parents atopic w identical manifestation 50 - 80%
one affecrted parent 20 - 40%
one affected sibling 25 - 35%
PREVENTION
DURING PREGNANCY
- don’t smoke
- promote breastfeeding
AFTER BIRTH
- no smoking
- promote breastfeeding for 4-6 months
→ nb: little evidence for hydrolysed in allergy prevention
- solids by 4-6 months
- no evidence for delaying introduction of allergenic foods → may actually INCREASE risk
- DONT recommend maternal dietary restriction during preg or after → may actually INCREASE risk
ASCIA food guidelines food introduction in infants
What is skin prick testing good for?
ONLY IgE mediated allergies
so morbiliform rashes and delayed onset = not IgE so RAST wont identify it!
+ve skin test to penicillin = high risk of immediate or accelerated reaction
-ve SPT “” “” → extremely low risk
Cautious oral challenge under controlled conditions if SPT -ve
if no alternative to penicillin in proven allergy → needs desensitisation by specialist
Reactions to ampicillin/amoxicillin. cross reactibity w otjher abx?
Ampicillin/amoxicillin
Maculopap rash common
= 5 - 10% of children
100% if a/w EBV infection (mechanism unknown, not IgE mediated)
urticarial eruptions (itchy, migratory, often has edge to it)- more likely to be ALLERGIC ∴ so need to be referred for assessment
cephalosporin 3-7% cross reactivity
normal frequency of infections in childhood?
age. number of infections <1 yo 6 infection 1-2yo 6 3-4. 5 5-9. 4 10-14. 3
NB: increased infections if mucopurulant = ABNORMAL
wide range of normality up to 12 infection/year
increased frequency w childcare, older siblings, exposure to tobacco smoke, allergic disease (apparent frequency)
10 warning signs for immunodeficiency
1) 4+ ear infections within 1 year, esp if discharge
2) 2+ serious sinus infections within 1 year
3) 2+ months on Abx with little effect
4) 2+ pneumonias within 1 year
5) FFT - weight or growth
6) recurrent deep skin or organ abscesses
7) persistent thrush in mouth or skin after age 1 yo (out of context of recent antis)
8) need for IV abx to clear infections
9) 2+ deep seated infections eg: meningitis, OM, cellulitis, or sepsis
10 FHx immune deficiency
Clinical infections w likely immuno deficiency
HUMORAL
Recurrent sinopulmonary infections, chronic diarrhoea + FTT
- less common = arthritis, hepatitis, coeliac, IBD
CELLULAR
recurrent fungal infections, opportunistic infections, chronic diarrhoea, FTT, neonatal hypoCa
PHAGOCYTIC
recurrent periodontal dz, gingivitis, skin + deep abscesses, fungal pneumonia, OM
COMPLEMENT
recurrent bacteraemia, severe or disseminated pneumococcal or meningococcal infection, autoimmunity, vasculitis
